Three-Dimensional Delayed-Enhanced Cardiac MRI Reconstructions to Guide Ventricular Tachycardia Ablations and Assess Ablation Lesions
2012; Lippincott Williams & Wilkins; Volume: 5; Issue: 2 Linguagem: Inglês
10.1161/circep.111.968636
ISSN1941-3149
AutoresJing Tian, Ghada Ahmad, Olurotimi Mesubi, Jean Jeudy, Timm Dickfeld,
Tópico(s)Atrial Fibrillation Management and Outcomes
ResumoHomeCirculation: Arrhythmia and ElectrophysiologyVol. 5, No. 2Three-Dimensional Delayed-Enhanced Cardiac MRI Reconstructions to Guide Ventricular Tachycardia Ablations and Assess Ablation Lesions Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBThree-Dimensional Delayed-Enhanced Cardiac MRI Reconstructions to Guide Ventricular Tachycardia Ablations and Assess Ablation Lesions Jing Tian, MD, PhD, Ghada Ahmad, MD, Olurotimi Mesubi, MD, MPH, Jean Jeudy, MD and Timm Dickfeld, MD, PhD Jing TianJing Tian From the University of Maryland School of Medicine (J.T., G.A., O.M., J.J., T.D.) and Baltimore VA Medical Center (T.D.), Baltimore, MD. , Ghada AhmadGhada Ahmad From the University of Maryland School of Medicine (J.T., G.A., O.M., J.J., T.D.) and Baltimore VA Medical Center (T.D.), Baltimore, MD. , Olurotimi MesubiOlurotimi Mesubi From the University of Maryland School of Medicine (J.T., G.A., O.M., J.J., T.D.) and Baltimore VA Medical Center (T.D.), Baltimore, MD. , Jean JeudyJean Jeudy From the University of Maryland School of Medicine (J.T., G.A., O.M., J.J., T.D.) and Baltimore VA Medical Center (T.D.), Baltimore, MD. and Timm DickfeldTimm Dickfeld From the University of Maryland School of Medicine (J.T., G.A., O.M., J.J., T.D.) and Baltimore VA Medical Center (T.D.), Baltimore, MD. Originally published1 Apr 2012https://doi.org/10.1161/CIRCEP.111.968636Circulation: Arrhythmia and Electrophysiology. 2012;5:e31–e35IntroductionVoltage mapping is the primary tool for identifying sites for substrate-guided ventricular tachycardia (VT) ablation, but there are limitations in its application. Delayed-enhanced cardiac MRI (DE-CMRI) can facilitate VT ablations by providing complementary detail about myocardial scar location and geometry. We present the case of a patient with recurrent VT with left bundle branch block (LBBB)-right-side inferior axis morphology and a challenging voltage map.CaseThe patient was a 76-year-old man with a history of hypertension, type 2 diabetes mellitus, atrial fibrillation, and newly diagnosed dilated nonischemic cardiomyopathy (ejection fraction, 30%). He was transferred to our facility because of multiple episodes of monomorphic VT with a heart rate of 160 beats/min and an LBBB-right-side inferior axis morphology (Figure 1) consistent with an origin in the right ventricular outflow tract (RVOT). He required 2 episodes of electric cardioversion and amiodarone therapy, but the VT was refractory to amiodarone, so the patient underwent a VT ablation procedure.Download figureDownload PowerPointFigure 1. Clinical ventricular tachycardia with left bundle branch block-right-side inferior axis morphology.CMRI with a 1.5-T Siemens Avanto scanner was performed in multiple anatomic planes using T1-weighted and cine steady-state free precision sequences. Gadolinium-enhanced sequences to evaluate early myocardial perfusion and delayed myocardial enhancement were also performed, using 0.1 mL/kg gadobenate dimeglumine. DE-CMRI demonstrated midmyocardial scar in the anteroseptal region of the RVOT (Figure 2), which raised the possibility of a substrate-mediated VT.Download figureDownload PowerPointFigure 2. Preablation 2D delayed-enhanced cardiac MRI. Preablation short-axis views from base to apex, showing delayed gadolinium enhancement corresponding to midseptal scar in the anteroseptal area of the right ventricular outflow tract (arrows).Reformatted 2D slices using Amira software allowed the reconstruction of 3D models of the right ventricle (RV) and left ventricle (LV) anatomy with embedded myocardial scar. These were exported as 3D Carto-readable mesh files and allowed the identification of mapping point positions on the corresponding 2D images. MRI surfaces were uploaded into the clinical CartoMERGE system (Biosense).RV and LV voltage maps were created using the CartoMERGE system and a 3.5-mm Navistar cooled-tip catheter (Biosense Webster) with a filling threshold of 15 mm. The 3D DE-CMRI reconstructions were coregistered as previously described, using the commercial visual alignment and surface registration algorithms.1 Standard clinical voltage criteria were used to define scar ( 1.5 mV) myocardium.2 A bipolar endocardial RV and LV voltage map revealed no endocardial scar (Figure 3).Download figureDownload PowerPointFigure 3. Three-dimensional voltage map of the right and left ventricles demonstrates normal endocardial voltage (red, 1.5 mV).Using programmed electric stimulation, VT was easily inducible, with a tachycardia cycle length of 418 ms (LBBB-right-side inferior axis morphology). Activation mapping demonstrated earliest activation in the high septal outflow tract but was limited because of self-termination. The normal LV and RV voltage maps and 12-lead VT morphology raised the question of a more benign RVOT tachycardia mechanism occurring coincidentally in this patient with newly diagnosed nonischemic cardiomyopathy. However, the integrated scar substrate in the anteroseptal RVOT suggested a scar-mediated reentrant VT and directed the pace mapping to the area of midmyocardial delayed enhancement, where a 12/12 pace map match was found (Figure 4). Ablation at the superior border of the septal scar (30–50 W; total ablation time, 297 s) resulted in noninducibility of the VT with programmed electric stimulation of up to triple extrastimuli both on and off isoproterenol as well as burst pacing.Download figureDownload PowerPointFigure 4. Twelve-lead surface ECG shows the clinical VT with corresponding 12/12 pace match (left bundle branch block right inferior axis QRS morphology). This corresponded to the site of successful ablation.Postablation DE-CMRI performed 24 hours later as part of a research study demonstrated ablation lesions as distinct areas of nonreflow reaching into the area of previously observed midmyocardial MRI scar (Figure 5). Two days after the VT ablation, the patient had an implantable cardioverter-defibrillator (ICD) implanted for secondary prevention. During a 6-month follow-up period, the patient remained off antiarrhythmic drugs and has not experienced any episodes of ventricular arrhythmia.Download figureDownload PowerPointFigure 5. Postablation MRI and integration with 3D map. Postablation 2D delay-enhanced cardiac MRI short-axis view demonstrates the midmyocardial septal scar (A) with two nonreflow areas corresponding to ablation lesions (B). The 3D reconstruction of the MRI image was then superimposed with the voltage map. The blue area represents the midmyocardial septal scar (A); ablation lesions reconstructed in orange (B) are localized at same location as the corresponding ablation points in the voltage map (brown) (C).Discussion and Teaching PointsRVOT TachycardiaRVOT tachycardia is the predominant form of idiopathic VT, and the cellular mechanism is believed to be triggered by c-AMP-mediated delayed afterdepolarization activity induced by catecholamines. Patients generally do not have structural heart disease. In 90% of cases, it manifests as repetitive monomorphic nonsustained VT or paroxysmal exercise-induced sustained VT.3 The morphology of RVOT VT is monomorphic with an LBBB pattern and a left- or right-side inferior frontal plane axis. There appears to be an equal male-to-female distribution, and the majority of patients are aged 30 to 50 years, although the age range can span from 6 to 77 years.3 This condition has an excellent prognosis with no requirement for ICD implantation. Although patients with no or infrequent symptoms may require no treatment, the treatment of choice for VT-associated symptoms, such as presyncope or syncope, is radiofrequency ablation. Successful ablation rates are in the 90% to 95% range, with minimal complication rates. 3,4 Alternatively, antiarrhythmic agents, such as β-blockers, calcium channel blockers, and class I and III antiarrhythmic agents, can be used. Although the prevalence of c-AMP-triggered RVOT-type VT in patients with a normal voltage map and cardiomyopathy is not known, the presence of a cardiomyopathy should always raise strong concerns about a scar-mediated reentrant VT.CMRI Detection of Scar-Related VT SubstrateCMRI is considered the current gold standard to image cardiac fibrosis or scarring. An excellent correlation between CMRI scar and histological examination has been shown in canine studies.5 CMRI allows for high-resolution evaluation of the RV anatomy, tissue characterization, and wall motion abnormalities to rule out other structural abnormalities, such as arrhythmogenic right ventricular cardiomyopathy.In the present patient, although the 12-lead morphology, VT origin, and normal voltage map were compatible with a triggered outflow tract tachycardia, the cardiomyopathy and presence of myocardial scar on DE-CMRI as well as induction with programmed electric stimulation indicated a substrate-related reentrant mechanism. It is important to point out that the midmyocardial scar was not detected by bipolar voltage mapping from the RV or LV, which may have been due to the myocardial thickness because endocardial layers of ≥2-mm thickness frequently result in bipolar voltage values of >1.5 mV.1The reconstructed and integrated DE-CMRI scar directed the pace mapping to the area of midmyocardial scar and resulted in the rapid identification of the best 12/12 pace map site. Importantly, it provided a rationale to ablate in an area of preserved voltage because the underlying scar substrate had been confirmed.CMRI Characterization of Ablation Lesion Relative to Scar SubstrateThe matched location of CMRI substrate and the successful ablation site confirmed the likely substrate-based reentrant mechanism. Additionally, the visualization of the ablation extending into the area of scar provided confirmation that a sufficiently large ablation lesion to alter the scar substrate had been created and that scar modification had been performed. Such a combination of intramyocardial scar and normal voltage might provide an explanation for the location of ≈4% of successful ablation sites within healthy myocardium as defined by voltage mapping.6Recently, Ilg et al6 demonstrated the feasibility of visualizing ablation lesions with DE-CMRI as delayed enhancement in human myocardium without any preexisting fibrosis. However, the visualization of ablation lesions in areas of fibrosis might be more difficult, with DE-CMRI akin to trying to image a white lesion within white myocardium. A possible solution could be the more pronounced degree of nonreperfusion created by the ablation lesion. Ablation results in a complete loss of cellular and vascular architecture. Although residual vascularity in scar-related fibrosis results mostly in a white enhancement pattern, ventricular ablation lesions demonstrate initially a dark area of nonreflow, as has been shown in animal studies.7 This case demonstrates that such an approach might be feasible in human cases.Take-Home MessageAlthough an LBBB inferior axis VT morphology and normal voltage map is consistent with a triggered RVOT VT mechanism, the presence of structural heart disease always requires assessment of scar-mediated VT. DE-CMRI is capable of detecting myocardial fibrosis not identified by voltage mapping (pointing toward a reentrant mechanism), defining the ablation target, and providing visual feedback about the ablation success.Sources of FundingThis work was supported by a Scientist Development Grant (0635304N to T.D.) by the American Heart Association.DisclosuresDr Dickfeld receives support from Biosense-Webster for research and consulting services.Footnotes*These authors contributed equally in this work.Correspondence to Timm Dickfeld, MD, PhD, Division of Cardiology, University of Maryland School of Medicine, 22 S Greene St, N3W77, Baltimore, MD 21201. E-mail [email protected]umaryland.eduReferences1. Dickfeld T, Tian J, Ahmad G, Jimenez A, Turgeman A, Kuk R, Peters M, Saliaris A, Saba M, Shorofsky S, Jeudy J. MRI-guided ventricular tachycardia ablation: integration of late gadolinium-enhanced 3D scar in patients with implantable cardioverter-defibrillators. Circ Arrhythm Electrophysiol. 2011; 4:172–184.LinkGoogle Scholar2. Marchlinski FE, Callans DJ, Gottlieb CD, Zado E. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation. 2000; 101:1288–1296.LinkGoogle Scholar3. Lerman BB, Stein KM, Markowitz SM. Idiopathic right ventricular outflow tract tachycardia: a clinical approach. Pacing Clin Electrophysiol. 1996; 19:2120–2137.CrossrefMedlineGoogle Scholar4. Joshi S, Wilber DJ. Ablation of idiopathic right ventricular outflow tract tachycardia: current perspectives. J Cardiovasc Electrophysiol. 2005; 16:S52–S58.CrossrefMedlineGoogle Scholar5. Kim RJ, Fieno DS, Parrish TB, Harris K, Chen EL, Simonetti O, Bundy J, Finn JP, Klocke FJ, Judd RM. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation. 1999; 100:1992–2002.LinkGoogle Scholar6. Ilg K, Baman TS, Gupta SK, Swanson S, Good E, Chugh A, Jongnarangsin K, Pelosi F, Crawford T, Oral H, Morady F, Bogun F. Assessment of radiofrequency ablation lesions by CMR imaging after ablation of idiopathic ventricular arrhythmias. J Am Coll Cardiol Cardiovsc Imaging. 2010; 3:278–285.CrossrefMedlineGoogle Scholar7. Dickfeld T, Kato R, Zviman M, Lai S, Meininger G, Lardo AC, Roguin A, Blumke D, Berger R, Calkins H, Halperin H. Characterization of radiofrequency ablation lesions with gadolinium-enhanced cardiovascular magnetic resonance imaging. J Am Coll Cardiol. 2006; 47:370–378.CrossrefMedlineGoogle ScholarEditor's PerspectiveThis teaching rounds case makes several interesting points. First, ventricular tachycardias (VTs) that originate from scar in the superior septum or outflow region can have an electrocardiographic appearance mimicking idiopathic VT. Second, a normal bipolar voltage map, as defined by an electrogram amplitude >1.5 mV, does not exclude the presence of scar deep into the endocardium. Third, it illustrates how imaging to detect scar can potentially help to guide an ablation procedure and may at some point be useful for assessing ablation lesions. These points are amplified herein.Most sustained monomorphic VTs in structural disease are due to scar-related reentry.1 Rarely is an idiopathic VT found in a patient with structural heart disease, such as an idiopathic right ventricular outflow tract VT in a patient with hypertrophic cardiomyopathy.2 Although idiopathic VT cannot be absolutely excluded in this case, the proximity of the successful ablation site to the scar and inducibility by programmed stimulation favor a scar-related VT. Assessment of entrainment would have been interesting if it were possible. Entrainment would further support scar-related reentry rather than idiopathic VT, which usually behaves in a manner more consistent with triggered automaticity.Despite its association with a scar, the electrocardiographic appearance of the VT is consistent with idiopathic VT. Electrocardiographic features of left bundle branch block-like VTs that are associated with scar rather than idiopathic VT include transition after V4, notched downstroke in V1 or V2, and QRS onset to nadir of S wave in V1 of >90 ms.3 The present VT lacks these features. The case exemplifies the limitation of electrocardiography, which by itself is not a sufficiently reliable indication that VT is not associated with scar. An apparently idiopathic VT usually warrants additional imaging to provide further reassurance that structural disease is absent.The current bipolar voltage map was normal by present standards, another factor that supports idiopathic VT rather than scar-related VT. A bipolar amplitude of >1.5 mV is now widely accepted as the lower limit of normal.4 It is important to recognize, however, the limitations of voltage mapping. Marchlinski and coworkers5 codified the 1.5-mV standard from mapping studies using catheters with 4-mm-tip electrodes separated by 1 mm from a smaller ring electrode. Signals were filtered at 10 to 400 Hz on an electroanatomic mapping system. They mapped 4 right and 4 left ventricles in 6 subjects, finding that 95% of electrograms had an amplitude of >1.55 mV in the left ventricle, whereas the corresponding cut point of 95% of electrograms in the normal right ventricle was >1.44 mV. Marchlinski et al suggested a 1.5-mV threshold for clinical use. This value has held up remarkably well in different studies for identifying scar in animal models of infarction and in humans, despite some differences in recording systems and recording catheters (eg, 3.5-mm rather than 4-mm distal electrode). It is apparent, however, that this is a conservative definition of scar; that is, it is specific but has limited sensitivity.MRI is beginning to define some of these limitations.6–8 Wijnmaalen and coworkers6 compared voltage maps with MRI in patients with prior myocardial infarction. They found excellent correlation of scar, in general, but several patients with marked discrepancies had nontransmural areas of scar that were not appreciated by voltage maps. Dickfeld and colleagues7 also found that a bipolar endocardial voltage map with a threshold of 1.5 mV will not detect areas of intramural and epicardial scar that does not extend to within 2 mm of the endocardium. More recently, Hutchinson and coworkers9 exploited the presence of greater far-field signal content in unipolar recordings that increases the field of view to develop voltage criteria for unipolar, minimally filtered electrograms that suggest the presence of epicardial, and potentially intramural, scar. Whether a unipolar voltage map would have detected the intramural scar in the present case is not known. Further studies correlating imaging with electrogram characteristics should continue to refine the ability to detect intramural and epicardial scar to help to guide ablation. Detection of epicardial scar is particularly relevant when arrhythmogenic right ventricular cardiomyopathy is suspected because the electrophysiological abnormalities in this disease often are more extensive in the epicardium than in the endocardium, and epicardial ablation often is required.10MRI is a powerful tool that allows visualization of scar and potentially of radiofrequency lesions. The ability to integrate MRIs with electroanatomic mapping systems in the electrophysiology laboratory will continue to provide insights into the pathophysiology of arrhythmias.7 Unfortunately, many patients who could benefit from this approach have implantable cardioverter-defibrillators (ICDs) that preclude imaging at many centers. When it can be performed, the presence of an ICD degrades the image quality of some regions of the heart.7 Thus, additional methods for imaging scar are of interest.11The present patient likely had a scar-related VT. The etiology of scar is not known, but a myopathic process or infiltrative disease, such as sarcoidosis, is possible. Although no VT was inducible after ablation, he received an ICD. Guidelines recommend ICD implantation for "patients with structural heart disease and spontaneous sustained VT, whether hemodynamically stable or unstable."12 Data that ICDs improve the rate of mortality in patients with hemodynamically tolerated VT are lacking. It is recognized, however, that the type of cardiac disease is not known and may be progressive. Furthermore, the acute results of programmed stimulation after ablation of scar-related VT have been poorly predictive of long-term outcome in many studies.1 The ICD provides potential termination of stable VT by antitachycardia pacing as well as protection against life-threatening VTs if these develop.References1. Aliot EM, Stevenson WG, Almendral-Garrote JM, Bogun F, Calkins CH, Delacretaz E, Della Bella P, Hindricks G, Jais P, Josephson ME, Kautzner J, Kay GN, Kuck KH, Lerman BB, Marchlinski F, Reddy V, Schalij MJ, Schilling R, Soejima K, Wilber D. EHRA/HRS expert consensus on catheter ablation of ventricular arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). Heart Rhythm. 2009; 6:886–933.CrossrefMedlineGoogle Scholar2. Inada K, Seiler J, Roberts-Thomson KC, Steven D, Rosman J, John RM, Sobieszczyk P, Stevenson WG, Tedrow UB. Substrate characterization and catheter ablation for monomorphic ventricular tachycardia in patients with apical hypertrophic cardiomyopathy. J Cardiovasc Electrophysiol. 2011; 22:41–48.CrossrefMedlineGoogle Scholar3. Wijnmaalen AP, Stevenson WG, Schalij MJ, Field ME, Stephenson K, Tedrow UB, Koplan BA, Putter H, Epstein LM, Zeppenfeld K. ECG identification of scar-related ventricular tachycardia with a left bundle-branch block configuration. Circ Arrhythm Electrophysiol. 2011; 4:486–493.LinkGoogle Scholar4. Del Carpio Munoz F, Buescher TL, Asirvatham SJ. Teaching points with 3-dimensional mapping of cardiac arrhythmia: how to overcome potential pitfalls during substrate mapping?Circ Arrhythm Electrophysiol. 2011; 4:e72-e75.LinkGoogle Scholar5. Marchlinski FE, Callans DJ, Gottlieb CD, Zado E. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation. 2000; 101:1288–1296.LinkGoogle Scholar6. Wijnmaalen AP, van der Geest RJ, van Huls van Taxis CF, Siebelink HM, Kroft LJ, Bax JJ, Reiber JH, Schalij MJ, Zeppenfeld K. Head-to-head comparison of contrast-enhanced magnetic resonance imaging and electroanatomical voltage mapping to assess post-infarct scar characteristics in patients with ventricular tachycardias: real-time image integration and reversed registration. Eur Heart J. 2011; 32:104–114.CrossrefMedlineGoogle Scholar7. Dickfeld T, Tian J, Ahmad G, Jimenez A, Turgeman A, Kuk R, Peters M, Saliaris A, Saba M, Shorofsky S, Jeudy J. MRI-guided ventricular tachycardia ablation: integration of late gadolinium-enhanced 3D scar in patients with implantable cardioverter-defibrillators. Circ Arrhythm Electrophysiol. 2011; 4:172–184.LinkGoogle Scholar8. Bogun FM, Desjardins B, Good E, Gupta S, Crawford T, Oral H, Ebinger M, Pelosi F, Chugh A, Jongnarangsin K, Morady F. Delayed-enhanced magnetic resonance imaging in nonischemic cardiomyopathy: utility for identifying the ventricular arrhythmia substrate. J Am Coll Cardiol. 2009; 53:1138–1145.CrossrefMedlineGoogle Scholar9. Hutchinson MD, Gerstenfeld EP, Desjardins B, Bala R, Riley MP, Garcia FC, Dixit S, Lin D, Tzou WS, Cooper JM, Verdino RJ, Callans DJ, Marchlinski FE. Endocardial unipolar voltage mapping to detect epicardial ventricular tachycardia substrate in patients with nonischemic left ventricular cardiomyopathy. Circ Arrhythm Electrophysiol. 2011; 4:49–55.LinkGoogle Scholar10. Garcia FC, Bazan V, Zado ES, Ren JF, Marchlinski FE. Epicardial substrate and outcome with epicardial ablation of ventricular tachycardia in arrhythmogenic right ventricular cardiomyopathy/dysplasia. Circulation. 2009; 120:366–375.LinkGoogle Scholar11. Tian J, Jeudy J, Smith MF, Jimenez A, Yin X, Bruce PA, Lei P, Turgeman A, Abbo A, Shekhar R, Saba M, Shorofsky S, Dickfeld T. Three-dimensional contrast-enhanced multidetector CT for anatomic, dynamic, and perfusion characterization of abnormal myocardium to guide ventricular tachycardia ablations. Circ Arrhythm Electrophysiol. 2010; 3:496–504.LinkGoogle Scholar12. Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Smith SC, Jacobs AK, Adams CD, Anderson JL, Buller CE, Creager MA, Ettinger SM, Faxon DP, Halperin JL, Hiratzka LF, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura RA, Ornato JP, Riegel B, Tarkington LG, Yancy CW. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. Circulation. 2008; 117:e350-e408.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Schleberger R, Riess J, Brauer A, Pinnschmidt H, Rottner L, Moser F, Moser J, Kany S, My I, Lemoine M, Reissmann B, Meyer C, Metzner A, Ouyang F, Kirchhof P and Rillig A (2022) Ablation of Outflow Tract Arrhythmias in Patients With and Without Structural Heart Disease—A Comparative Analysis, Frontiers in Cardiovascular Medicine, 10.3389/fcvm.2022.910042, 9 Schleberger R, Jularic M, Salzbrunn T, Hacke C, Schwarzl J, Hoffmann B, Steven D, Willems S, Lemoine M and Meyer C (2020) Outcome of catheter ablation of non-reentrant ventricular arrhythmias in patients with and without structural heart disease, European Journal of Medical Research, 10.1186/s40001-020-0400-y, 25:1, Online publication date: 1-Dec-2020. Vunnam R, Maheshwari V, Jeudy J, Ghzally Y, Imanli H, Abdulghani M, Mahat J, Timilsina S, Restrepo A, See V, Shorofsky S and Dickfeld T (2020) Ventricular arrhythmia ablation lesions detectability and temporal changes on cardiac magnetic resonance, Pacing and Clinical Electrophysiology, 10.1111/pace.13886, 43:3, (314-321), Online publication date: 1-Mar-2020. Imanli H, Ume K, Jeudy J, Bob-Manuel T, Smith M, Chen W, Abdulghani M, Ghzally Y, Mahat J, Itah R, Restrepo A, See V, Shorofsky S, Dilsizian V and Dickfeld T (2018) Ventricular Tachycardia (VT) Substrate Characteristics: Insights from Multimodality Structural and Functional Imaging of the VT Substrate Using Cardiac MRI Scar, 123 I-Metaiodobenzylguanidine SPECT Innervation, and Bipolar Voltage , Journal of Nuclear Medicine, 10.2967/jnumed.118.211698, 60:1, (79-85), Online publication date: 1-Jan-2019. Ibrahim E, Runge M, Stojanovska J, Agarwal P, Ghadimi-Mahani M, Attili A, Chenevert T, Harder C and Bogun F (2018) Optimized cardiac magnetic resonance imaging inversion recovery sequence for metal artifact reduction and accurate myocardial scar assessment in patients with cardiac implantable electronic devices, World Journal of Radiology, 10.4329/wjr.v10.i9.100, 10:9, (100-107), Online publication date: 28-Sep-2018. Baldinger S, Tedrow U and Stevenson W (2017) Ventricular Tachycardia Ablation Cardiac Arrhythmias, Pacing and Sudden Death, 10.1007/978-3-319-58000-5_13, (157-172), . Lee N and Litt H (2016) Imaging of patients with implanted devices and arrhythmia, South African Journal of Radiology, 10.4102/sajr.v20i2.1046, 20:2 Ranjan R, McGann C, Jeong E, Hong K, Kholmovski E, Blauer J, Wilson B, Marrouche N and Kim D (2014) Wideband late gadolinium enhanced magnetic resonance imaging for imaging myocardial scar without image artefacts induced by implantable cardioverter-defibrillator: a feasibility study at 3 T, Europace, 10.1093/europace/euu263, 17:3, (483-488), Online publication date: 1-Mar-2015. Grothoff M, Piorkowski C, Eitel C, Gaspar T, Lehmkuhl L, Lücke C, Hoffmann J, Hildebrand L, Wedan S, Lloyd T, Sunnarborg D, Schnackenburg B, Hindricks G, Sommer P and Gutberlet M (2014) MR Imaging–guided Electrophysiological Ablation Studies in Humans with Passive Catheter Tracking: Initial Results, Radiology, 10.1148/radiol.13122671, 271:3, (695-702), Online publication date: 1-Jun-2014. Stevens S, Tung R, Rashid S, Gima J, Cote S, Pavez G, Khan S, Ennis D, Finn J, Boyle N, Shivkumar K and Hu P (2014) Device artifact reduction for magnetic resonance imaging of patients with implantable cardioverter-defibrillators and ventricular tachycardia: Late gadolinium enhancement correlation with electroanatomic mapping, Heart Rhythm, 10.1016/j.hrthm.2013.10.032, 11:2, (289-298), Online publication date: 1-Feb-2014. Rashid S, Rapacchi S, Vaseghi M, Tung R, Shivkumar K, Finn J and Hu P (2014) Improved Late Gadolinium Enhancement MR Imaging for Patients with Implanted Cardiac Devices, Radiology, 10.1148/radiol.13130942, 270:1, (269-274), Online publication date: 1-Jan-2014. Ashikaga H, Kolandaivelu A, Nazarian S and Halperin H (2014) CT and MRI for Electrophysiology Cardiac Electrophysiology: From Cell to Bedside, 10.1016/B978-1-4557-2856-5.00061-3, (595-603), . Piers S, Tao Q, van Huls van Taxis C, Schalij M, van der Geest R and Zeppenfeld K (2013) Contrast-Enhanced MRI–Derived Scar Patterns and Associated Ventricular Tachycardias in Nonischemic Cardiomyopathy, Circulation: Arrhythmia and Electrophysiology, 6:5, (875-883), Online publication date: 1-Oct-2013. Klein T, Dilsizian V, Cao Q, Chen W and Dickfeld T (2013) The Potential Role of Iodine-123 Metaiodobenzylguanidine Imaging for Identifying Sustained Ventricular Tachycardia in Patients with Cardiomyopathy, Current Cardiology Reports, 10.1007/s11886-013-0359-1, 15:5, Online publication date: 1-May-2013. April 2012Vol 5, Issue 2 Advertisement Article InformationMetrics © 2012 American Heart Association, Inc.https://doi.org/10.1161/CIRCEP.111.968636PMID: 22511662 Manuscript receivedApril 1, 2011Manuscript acceptedDecember 22, 2011Originally publishedApril 1, 2012 Keywordsmagnetic resonance imagingtachycardia ventricularcatheter ablationPDF download Advertisement SubjectsArrhythmiasCatheter Ablation and Implantable Cardioverter-DefibrillatorComputerized Tomography (CT)Electrophysiology
Referência(s)